Venous Occlusive Disease

Venous Occlusive Disease

Description, Causes and Risk Factors:

The retina requires a rich blood supply. Arteries carry oxygenated blood from the heart to the retina and veins carry deoxygenated blood from the retina back to the heart via the optic nerve. The retinal arteries may thicken and become stiff with age, especially in persons with high blood pressure, elevated cholesterol/triglycerides or diabetes. The retinal arteries and veins are in close proximity within the optic nerve and cross at multiple locations on the surface of the retina. Thickening of the arteries can compress the retinal vein either in the optic nerve or where the arteries cross the veins. Sometimes the arteries compress the veins so much that the blood flow in the vein is interrupted and cannot flow back to the heart. This causes blood to back up in the retina much like water backs up in a bathtub with a clogged drain. The increased pressure of blood in the veins causes bleeding and swelling in the retina. There are three variations of retinal vein occlusions. The most common is a branch retinal vein occlusion where a retinal vein is blocked on the surface of the retina. The resultant hemorrhaging and swelling can cause decreased vision if the center of the retina (the macula) is involved. The second most common is a central retinal vein occlusion where the retinal vein becomes blocked within the optic nerve. Central retinal vein occlusions are typically more severe and causing hemorrhages and swelling throughout the retinal leading to more profound decrease in vision. The least common venous occlusion is a hemi-retinal vein occlusion where the vein draining one-half of the venous circulation is occluded. This is typically less severe than a central retinal vein occlusion but worse than a branch retinal vein occlusion.

Occlusion of the central retinal vein is probably a result of both local and systemic causes. The actual mechanisms producing the clinical picture of central retinal vein occlusion may be roughly divided into those conditions that produce a physical blockage at the level of the lamina cribrosa, and those conditions in which hemodynamic factors result in an obstruction to the flow of blood. These mechanisms probably coexist in many patients with central retinal vein occlusion.

The pathogenesis of this condition and the underlying histopathology have remained controversial ever since Michel first correlated the clinical appearance with the histopathology. The fact that relatively few eyes have been histopathologically examined during the freshly obstructed stage has contributed to the problem. Many of the reported cases have involved eyes that were enucleated because of longstanding neovascular glaucoma; secondary changes that did not play a role in the original occlusion may have occurred in these eyes.

The precise etiology of central retinal vein occlusion is not entirely clear. There are now some clues as to the conditions associated with this condition. Many published articles have reported on the association between central retinal vein occlusion and some other condition, whether systemic or ocular. Although some of these associated conditions probably are, in some cases, related to central retinal vein occlusion, there is no way to determine in most cases whether the association is only coincidental on the basis of single-case reports.

The risk factors for the development of VOD are as follows:

    Veno occlusive disease (VOD) is also associated with other toxins such as alcohol, oral contraceptives, toxic oil, terbina?ne, or radiation injury.

  • Abnormal liver function, in particular a raised AST, prior to SCT.

  • Previous liver disease.

  • Previous abdominal irradiation.

  • Busulphan containing conditioning regime.

  • Unrelated donor transplant.

  • Previous Mylotarg.

  • Pre existing liver disease (hepatitis C, previous ?brosis, hypertransaminasemia).

  • Previous exposure to a myeloablative regimen.

  • Past history of HSOS.

  • Use of myeloablative regimen.

  • High dose of total body irradiation.

  • Use of cyclophosphamide containing regimes.

  • Administration of cyclophosphamide after busulfan.

  • Fixed dose of Busulfan.

  • Use of oral rather than ev Busulfan.

  • Late timing of SCT in patients with leukaemia.

  • Carriers of haemocromathosis C282Y allele.


People who develop a venous occlusive disease typically have the sudden onset of blurred vision in one eye (there are many other ocular conditions which cause the sudden onset of blurred vision so an examination is needed to determine the cause). Some retinal vein occlusions have no symptoms.

    Classical VOD - this is characterized by jaundice, hepatomegaly +/-right upper quadrant pain and weight gain with edema and ascites. This occurs within the first two-three weeks after conditioning starts (D+1- D+14/D21).

  • Late VOD - this has the same clinical presentation as classical VOD but develops later (Day +30 onwards).

  • VOD with multi-organ failure - this has the same clinical presentation as classical and late VOD but with the addition of thrombocytopenia, pleural effusions, pulmonary infiltrates and/or progressive organ failure.


Certain laboratory studies may be useful in atypical cases (i.e., bilateral cases, those in young patients, those in patients with a personal or family history for thromboembolism). Determinations of the following may be helpful:

    Prothrombin time (PT) and activated partial thromboplastin time (aPTT).

  • Protein C, protein S, factor V Leiden, and antithrombin III.

  • Homocysteine.

  • Antinuclear antibody (ANA), lupus anticoagulant, and anticardiolipin.

  • Serum protein electrophoresis (SPEP) results.

Fluorescein angiography: A fluorescein angiogram is obtained as soon as the hemorrhages have cleared if the patient's vision is still depressed. The test is usually performed 3 months after the event. The purpose is to determine the cause of the visual loss (eg, macular edema, macular ischemia). If the visual loss is secondary to macular edema, laser photocoagulation in a grid pattern may be of benefit. Conversely, if macular ischemia is responsible for the visual loss, laser photocoagulation should not be offered.

Optical coherence tomography (OCT): Given its ability to measure retinal thickness in a quantitative fashion, OCT is a useful adjunct in the follow-up of patients with macular edema secondary to BRVO.

Histopathologic studies confirm the importance of arteriovenous crossings in the pathogenesis of this condition. Inner retinal ischemic atrophic areas have been described distal to the occlusion site. Variable degrees of arteriolar sclerosis have been reported. An intravascular fresh or recanalized thrombus is often found at the site of venous occlusion.


There a number of treatments which may help the vision in eyes with retinal vein occlusions. Laser photocoagulation for macular edema (swelling) may stabilize or improve vision. The injection of steroids or anti-VEGF drugs (anti-vascular endothelial cell growth factors) into the vitreous gel may also be used to treat macular edema associated with venous occlusive disease. Some eyes with venous occlusive disease develop the growth of abnormal, fragile blood vessels on the surface of the retina which can cause bleeding into the vitreous gel. Vitreous bleeding is usually associated with the sudden onset of floaters in the vision. Eyes with central retinal vein occlusions may also develop abnormal blood vessels on the iris which can cause a very severe form of glaucoma called neovascular glaucoma. Both neovascularization of the retina and iris are treated with scatter laser photocoagulation to the retina in the office. Retinal vein occlusions typically occur in only one eye so fortunately the vision in the fellow eye is unaffected. Since retinal vein occlusions are associated with hypertension, elevated cholesterol/triglycerides and diabetes, control of these medical conditions make venous occlusive disease less common.

NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.


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